JAX Mouse Strain Datasheet - 000693

WC/ReJ Kitl^Sl/J

Stock No:: 000693

Cryo Recovery

Overview

The spontaneous kit ligand; steel (Kitl^Sl) mutation behaves in a semidominant fashion causing deficiencies in pigment cells, germ cells, and blood cells.

Genetic overview

Genetic Background	Generation

Ahr^d

Allele Type	Gene Symbol	Gene Name
Not Applicable	Ahr	aryl-hydrocarbon receptor

Kitl^Sl

Allele Type	Gene Symbol	Gene Name
Spontaneous	Kitl	kit ligand

Allele Type	Gene Symbol	Gene Name
Spontaneous	Pde6b	phosphodiesterase 6B, cGMP, rod receptor, beta polypeptide

Research Applications

Metabolism Research
Research Tools
Cancer Research
Dermatology Research
Developmental Biology Research
Endocrine Deficiency Research
Immunology, Inflammation and Autoimmunity Research
Neurobiology Research

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Base Price

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$2,595.00 Domestic price Cryo Recovery

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Details

Important Note

This strain is homozygous for the retinal degeneration allele Pde6b^rd1. See article "Genetic Background Effects: Can Your Mice See?", JAX^® NOTES Spring 2002, No. 485.

Detailed Description

The multiple steel mutations (Kitl^Sl) behave in a semidominant fashion and cause deficiencies in pigment cells, germ cells, and blood cells paralleling those caused by the Kit locus mutations (dominant spotting alleles). Most of the alleles at steel locus cause severe anemia in utero and death by 15 to 16 days of gestation in homozygous mutant mice. However, compounds of two steel mutants (e.g. Kitl^Sl/Kitl^Sl-d) are viable, black-eyed white, are usually sterile in one or both sexes, and have severe macrocytic anemia. Heterozygous steel mice have a diluted coat color with a small amount of white spotting, are viable and fertile, and may have a slight macrocytic anemia. Primordial germ cells are absent in the nonviable steel homozygotes and severely reduced in steel heterozygotes. Mast cells are virtually absent in skin and other tissues of steel mutant mice. Tumors tend to develop in germ-cell-deficient ovaries with advancing age.

Development

Inbreeding started in 1948 from a heterozygous Kitl^W / + stock (same origin as the WB/ReJ strain). Kitl^sl (steel) mutation backcrossed to strain WB-+/+. Now maintained as a congenic strain for Kitl^sl.

Control Suggestions

Wild-type from the colony

Additional Information

Considerations for Choosing Controls

Selected References

Arguello F; Furlanetto RW; Baggs RB; Graves BT; Harwell SE; Cohen HJ; Frantz CN. 1992. Incidence and distribution of experimental metastases in mutant mice with defective organ microenvironments (genotypes Sl/Sld and W/Wv). Cancer Res 52(8):2304-9. PubMed: 1559233 MGI: J:468
Hayashi C; Sonoda T; Nakano T; Nakayama H; Kitamura Y. 1985. Mast-cell precursors in the skin of mouse embryos and their deficiency in embryos of Sl/Sld genotype. Dev Biol 109(1):234-41. PubMed: 3987963 MGI: J:7810
Huang E; Nocka K; Beier DR; Chu TY; Buck J; Lahm HW; Wellner D; Leder P; Besmer P. 1990. The hematopoietic growth factor KL is encoded by the Sl locus and is the ligand of the c-kit receptor, the gene product of the W locus. Cell 63(1):225-33. PubMed: 1698557 MGI: J:10751
Murphy ED. 1977. Effects of mutant steel alleles on leukemogenesis and life-span in the mouse. J Natl Cancer Inst 58(1):107-10. PubMed: 319242 MGI: J:5758
Shinohara T; Avarbock MR; Brinster RL. 2000. Functional analysis of spermatogonial stem cells in Steel and cryptorchid infertile mouse models. Dev Biol 220(2):401-11. PubMed: 10753526 MGI: J:61712
Zsebo KM; Williams DA; Geissler EN; Broudy VC; Martin FH; Atkins HL; Hsu RY; Birkett NC; Okino KH; Murdock DC; Jacobsen FW; Langley KE; Smith KA; Takeishi T; Cattanach BM; Galli SJ; Suggs SV. 1990. Stem cell factor is encoded at the Sl locus of the mouse and is the ligand for the c-kit tyrosine kinase receptor. Cell 63(1):213-24. PubMed: 1698556 MGI: J:10750

View All References

Genetics

Ahr^d

Allele Symbol: Ahr^d

Allele Name	d variant
Allele Type	Not Applicable
Allele Synonym(s)	Ah^d; Ah^k; AhRd; Ahhⁿ; ah; in
Gene Symbol and Name	Ahr, aryl-hydrocarbon receptor
Gene Synonym(s)	Ah; Ahh; Ahre; In; aromatic hydrocarbon responsiveness; aryl hydrocarbon hydroxylase; bHLHe76; dioxin receptor; inflammatory reactivity
Strain of Origin	Not Applicable
Chromosome	12
General Note	Strain of origin - this allele was found in DBA/2J, AKR/J, 129, SWR, RF, NZB strains
Molecular Note	This allele encodes a 104 kDa receptor that is stabilized by molybdate and has an affinity for ligand 10-100 fold lower than that of the receptor produced by the C57BL/6J allele. PCR sequencing of cDNA revealed ten nucleotide differences between the coding sequences of the DBA/2J and C57BL/6J receptors. Five of the ten differences would cause amino acid changes. One of these, an apparent T to C transition replaces the opal termination codon in the C57BL/6J allele with an arginine codon in the DBA/2J allele. This change would extend translation of the DBA/2J mRNA by 43 amino acids, accounting for the larger size of the peptide produced by this allele (104 kDa vs 95 kDa for the C57BL/6J allele). A second T to C transition changes a leucine codon in the C57BL/6J allele to a proline codon in the DBA/2J allele, and would likely change secondary structure of the peptide and thus ligand affinity.

Kitl^Sl

Allele Symbol: Kitl^Sl

Allele Name	steel
Allele Type	Spontaneous
Allele Synonym(s)	Mgf^Sl; Sl
Gene Symbol and Name	Kitl, kit ligand
Gene Synonym(s)	Clo; Con; DCUA; DFNA69; FPH2; FPHH; Gb; Gb; KL-1; Kitlg; MGF; Mgf; Mgf; SCF; SF; SHEP7; SLF; Sl; Sl; Steel; Steel factor; blaze; blz; blz; cloud gray; contrasted; grizzle-belly; grizzle-belly; mast cell growth factor; steel; stem cell factor
Strain of Origin	C3H
Chromosome	10
Molecular Note	By Southern blotting, it was concluded that this allele contains a deletion encompassing most, if not all, of the coding region of the gene. A probe corresponding to nucleotides 6 to 685 of the cDNA failed to hybridize to DNA obtained from embryos homozygous for this allele. PCR analysis with primers for sequences at various distances from the Kit gene narrowed the 5' and 3' deletion endpoints to a 350 and a 380 base-pair region, respectively. Sequencing of the product of PCR using primers designed to span the deletion revealed that it extends through 973,366 base pairs on Chromosome 10 between nucleotide positions 99,177,807 and 100,151,173 (NCBI Map Viewer, Build 36.1), with a 4-base pair insertion joining the deletion endpoints, and contains 6 predicted and 3 known genes.

Pde6b^rd1

Allele Symbol: Pde6b^rd1

Allele Name	retinal degeneration 1
Allele Type	Spontaneous
Allele Synonym(s)	Pdeb^rd1; rd; rd-1; rd1; rodless retina
Gene Symbol and Name	Pde6b, phosphodiesterase 6B, cGMP, rod receptor, beta polypeptide
Gene Synonym(s)	CSNB3; CSNBAD2; GMP-PDEbeta; PDEB; Pdeb; Pdeb; RP40; nmf137; phosphodiesterase, cGMP, rod receptor, beta polypeptide; r; r; rd; rd; rd-1; rd1; rd1; rd10; rd10; retinal degeneration; retinal degeneration 1; retinal degeneration 10
Strain of Origin	various
Chromosome	5
General Note	The following inbred strains are known to be homozygous for Pde6b: C3H sublines, CBA/J, FVB/NJ, PL/J, SB, SJL/J, and SWR/J.
Molecular Note	Two mutations have been identified in rd1 mice. A murine leukimia virus (Xmv-28) insertion in reverse orientation in intron 1 is found in all mouse strains with the rd1 phenotype. Further, a nonsense mutation (C to A transversion) in codon 347 that results in a truncation eliminating more than half of the predicted encoded protein, including the catalytic domain has also been identified in all rd1 strains of mice. A specific degradation of mutant transcript during or after pre-mRNA splicing is suggested.

Disease/Phenotype

Disease Terms

Research Areas By Genotype

This mouse can be used to support research in many areas including:

Genotype: Ahr^d related

Metabolism Research
Research Tools
- Toxicology Research

Genotype: Kitl^Sl related

Cancer Research
- Growth Factors/Receptors/Cytokines
- Increased Tumor Incidence
  - Gonadal Tumors
  - Gonadal Tumors: ovarian and testicular
Dermatology Research
- Color and White Spotting Defects
Developmental Biology Research
- Neural Crest Defects
Endocrine Deficiency Research
- Bone/Bone Marrow Defects
- Gonad Defects
- Hypothalamus/Pituitary Defects
- Skin Defects
Immunology, Inflammation and Autoimmunity Research
- Growth Factors/Receptors/Cytokines
- Immunodeficiency
  - Mast Cell Deficiency
Neurobiology Research
- Hearing Defects
Reproductive Biology Research
- Developmental Defects Affecting Gonads
  - germ cell deficient
- Fertility Defects
- Gonadal Tumors
  - ovarian and testicular
Research Tools
- Immunology, Inflammation and Autoimmunity Research
  - Mast Cell Deficiency
Sensorineural Research
- Hearing Defects

Genotype: Pde6b^rd1 related

Sensorineural Research
- Retinal Degeneration

Mammalian Phenotype Terms by Genotype

The following phenotype information is associated with a similar, but not exact match to this JAX^® Mice strain

Genotype: Kitl^Sl/Kitl⁺
either: (involves: C3H * WC) or (involves: C3H * C57BL/6 * DBA/2J * WC)

hematopoietic system phenotype

anemia
- mice are slightly anemic

decreased mast cell number
- heterozygotes have decreased mast cell numbers in dorsal skin compared to wild-type

immune system phenotype

decreased mast cell number
- heterozygotes have decreased mast cell numbers in dorsal skin compared to wild-type

Genotype: Kitl^Sl/Kitl⁺
involves: C3H

pigmentation phenotype

belly spot
- most mice have a white spot on the belly

decreased ear pigmentation
- mice have light ears

decreased foot pigmentation
- mice have light feet

diluted coat color
- affected mice have overall dilution of coat color, more extreme on the belly than back
- reduced coat color

head blaze
- very occasionally mice have a white blaze between their eyes

head spot
- most mice have a white spot on the belly

hematopoietic system phenotype

anemia
- mice display less severe anemia than homozygotes

decreased erythrocyte cell number
- at 7-13 days of age, red blood cell counts are 20-30% lower than wild-type

hearing/vestibular/ear phenotype

decreased ear pigmentation
- mice have light ears

reproductive system phenotype

reproductive system phenotype
- heterozygotes are viable and fertile

craniofacial phenotype

decreased ear pigmentation
- mice have light ears

integument phenotype

abnormal vibrissa morphology
- mice have light whiskers

belly spot
- most mice have a white spot on the belly

decreased ear pigmentation
- mice have light ears

decreased foot pigmentation
- mice have light feet

diluted coat color
- affected mice have overall dilution of coat color, more extreme on the belly than back
- reduced coat color

head blaze
- very occasionally mice have a white blaze between their eyes

head spot
- most mice have a white spot on the belly

pallor
- some pups after birth are pale compared to littermates

growth/size/body region phenotype

decreased ear pigmentation
- mice have light ears

Genotype: Kitl^Sl/Kitl⁺
involves: 129/Sv * C3H

endocrine/exocrine gland phenotype

increased testicular teratoma incidence
- incidence is 6.92% compared to ~2.6% in controls
- percentage is greater in second and subsequent litters compared to first litter or in first litter of older females compared to young mothers
- tumors are predominantly in left testis (71%) vs right (27%) or bilateral (2%)

reproductive system phenotype

increased testicular teratoma incidence
- incidence is 6.92% compared to ~2.6% in controls
- percentage is greater in second and subsequent litters compared to first litter or in first litter of older females compared to young mothers
- tumors are predominantly in left testis (71%) vs right (27%) or bilateral (2%)

neoplasm

increased testicular teratoma incidence
- incidence is 6.92% compared to ~2.6% in controls
- percentage is greater in second and subsequent litters compared to first litter or in first litter of older females compared to young mothers
- tumors are predominantly in left testis (71%) vs right (27%) or bilateral (2%)

increased tumor incidence
- male mice develop ~2-fold more tumors than controls

Genotype: Kitl^Sl/Kitl^Sl
involves: C3H

mortality/aging

lethality throughout fetal growth and development, complete penetrance
- an occasional mutant survives until birth
- no presumed homozygotes are born; homozygotes begin to die at ~E15-15.5 from anemia

nervous system phenotype

abnormal brain development
- at E10.5-12.5, small number of embryos, presumably homozygous, have brain abnormalities, including a collapsed brain, pseudoencephaly or a narrowed brain region
- from E14.5-17.5, some embryos show abnormal brain development (3/330) as described in younger embryos

myelencephalic blebs
- one E17.5 embryo displayed a bleb near the midline in the cervical region

spina bifida
- 4/330 embryos aged E14.5-17.5 displayed spina bifida

hematopoietic system phenotype

anemia
- starting around E13.5 and peaking at E14.5, presumed homozygotes display anemia recognized by overall paleness of the embryos

cardiovascular system phenotype

abnormal blood circulation
- in affected (anemic) animals, individual clumps or red blood cells can be seen in umbilical vessels; in controls, vessels are uniformly red with normal blood flow

reproductive system phenotype

infertility
- mice carrying two mutant alleles are sterile

pigmentation phenotype

absent skin pigmentation
- transplantation of skin grafts from E14, E15 and newborn mutants to normal siblings produced unpigmented hair

embryo phenotype

spina bifida
- 4/330 embryos aged E14.5-17.5 displayed spina bifida

integument phenotype

absent skin pigmentation
- transplantation of skin grafts from E14, E15 and newborn mutants to normal siblings produced unpigmented hair

pallor
- characteristic of anemic embryos

References

Arguello F; Furlanetto RW; Baggs RB; Graves BT; Harwell SE; Cohen HJ; Frantz CN. 1992. Incidence and distribution of experimental metastases in mutant mice with defective organ microenvironments (genotypes Sl/Sld and W/Wv). Cancer Res 52(8):2304-9. PubMed: 1559233 MGI: J:468
Hayashi C; Sonoda T; Nakano T; Nakayama H; Kitamura Y. 1985. Mast-cell precursors in the skin of mouse embryos and their deficiency in embryos of Sl/Sld genotype. Dev Biol 109(1):234-41. PubMed: 3987963 MGI: J:7810
Huang E; Nocka K; Beier DR; Chu TY; Buck J; Lahm HW; Wellner D; Leder P; Besmer P. 1990. The hematopoietic growth factor KL is encoded by the Sl locus and is the ligand of the c-kit receptor, the gene product of the W locus. Cell 63(1):225-33. PubMed: 1698557 MGI: J:10751
Murphy ED. 1977. Effects of mutant steel alleles on leukemogenesis and life-span in the mouse. J Natl Cancer Inst 58(1):107-10. PubMed: 319242 MGI: J:5758
Shinohara T; Avarbock MR; Brinster RL. 2000. Functional analysis of spermatogonial stem cells in Steel and cryptorchid infertile mouse models. Dev Biol 220(2):401-11. PubMed: 10753526 MGI: J:61712
Zsebo KM; Williams DA; Geissler EN; Broudy VC; Martin FH; Atkins HL; Hsu RY; Birkett NC; Okino KH; Murdock DC; Jacobsen FW; Langley KE; Smith KA; Takeishi T; Cattanach BM; Galli SJ; Suggs SV. 1990. Stem cell factor is encoded at the Sl locus of the mouse and is the ligand for the c-kit tyrosine kinase receptor. Cell 63(1):213-24. PubMed: 1698556 MGI: J:10750

Additional References

Chang B; Hawes NL; Hurd RE; Davisson MT; Nusinowitz S; Heckenlively JR. 2002. Retinal degeneration mutants in the mouse. Vision Res 42(4):517-25. PubMed: 11853768 MGI: J:75095
Poland A; Glover E. 1990. Characterization and strain distribution pattern of the murine Ah receptor specified by the Ahd and Ahb-3 alleles. Mol Pharmacol 38(3):306-12. PubMed: 2169579 MGI: J:34840
Schrott A; Egg G; Spoendlin H. 1988. Intermediate filaments in the cochleas of normal and mutant (w/wv, sl/sld) mice. Arch Otorhinolaryngol 245(4):250-4. PubMed: 2460075 MGI: J:9423
Wolf NS. 1978. Dissecting the hematopoietic microenvironment. II. The kinetics of the erythron of the S1/S1d mouse and the dual nature of its anemia. Cell Tissue Kinet 11(4):325-34. PubMed: 688326 MGI: J:6031

Additional - Ahr^d related

Benedict WF; Considine N; Nebert DW. 1973. Genetic differences in aryl hydrocarbon hydroxylase induction and benzo(a)pyrene-produced tumorigenesis in the mouse. Mol Pharmacol 9(2):266-77. PubMed: 4123113 MGI: J:84312
Boobis AR; Nebert DW. 1976. Genetic differences in the metabolism of carcinogens and in the binding of benzo (a) pyrene metabolites to DNA. Adv Enzyme Regul 15:339-62. PubMed: 1030186 MGI: J:12156
Castro DJ; Lohr CV; Fischer KA; Pereira CB; Williams DE. 2008. Lymphoma and lung cancer in offspring born to pregnant mice dosed with dibenzo[a,l]pyrene: the importance of in utero vs. lactational exposure. Toxicol Appl Pharmacol 233(3):454-8. PubMed: 18848954 MGI: J:143604
Chang C; Smith DR; Prasad VS; Sidman CL; Nebert DW; Puga A. 1993. Ten nucleotide differences, five of which cause amino acid changes, are associated with the Ah receptor locus polymorphism of C57BL/6 and DBA/2 mice. Pharmacogenetics 3(6):312-21. PubMed: 8148872 MGI: J:17460
Curran CP; Altenhofen E; Ashworth A; Brown A; Kamau-Cheggeh C; Curran M; Evans A; Floyd R; Fowler J; Garber H; Hays B; Kraemer S; Lang A; Mynhier A; Samuels A; Strohmaier C. 2012. Ahrd Cyp1a2(-/-) mice show increased susceptibility to PCB-induced developmental neurotoxicity. Neurotoxicology 33(6):1436-42. PubMed: 22935098 MGI: J:225088
Curran CP; Miller KA; Dalton TP; Vorhees CV; Miller ML; Shertzer HG; Nebert DW. 2006. Genetic differences in lethality of newborn mice treated in utero with coplanar versus non-coplanar hexabromobiphenyl. Toxicol Sci 89(2):454-64. PubMed: 16291824 MGI: J:113285
Curran CP; Nebert DW; Genter MB; Patel KV; Schaefer TL; Skelton MR; Williams MT; Vorhees CV. 2011. In utero and lactational exposure to PCBs in mice: adult offspring show altered learning and memory depending on Cyp1a2 and Ahr genotypes. Environ Health Perspect 119(9):1286-93. PubMed: 21571617 MGI: J:260665
Curran CP; Vorhees CV; Williams MT; Genter MB; Miller ML; Nebert DW. 2011. In utero and lactational exposure to a complex mixture of polychlorinated biphenyls: toxicity in pups dependent on the Cyp1a2 and Ahr genotypes. Toxicol Sci 119(1):189-208. PubMed: 20961953 MGI: J:260693
Felton JS; Nebert DW. 1975. Mutagenesis of certain activated carcinogens in vitro associated with genetically mediated increases in monooxygenase activity and cytochrome P 1-450. J Biol Chem 250(17):6769-78. PubMed: 808546 MGI: J:5564
Gielen JE; Goujon FM; Nebert DW. 1972. Genetic regulation of aryl hydrocarbon hydroxylase induction. II. Simple Mendelian expression in mouse tissues in vivo. J Biol Chem 247(4):1125-37. PubMed: 4110756 MGI: J:84250
Goujon FM; Nebert DW; Gielen JE. 1972. Genetic expression of aryl hydrocarbon hydroxylase induction. IV. Interaction of various compounds with different forms of cytochrome P-450 and the effect on benzo(a)pyrene metabolism in vitro. Mol Pharmacol 8(6):667-80. PubMed: 4118365 MGI: J:84252
Harper PA; Golas CL; Okey AB. 1991. Ah receptor in mice genetically nonresponsive for cytochrome P4501A1 induction: cytosolic Ah receptor, transformation to the nuclear binding state, and induction of aryl hydrocarbon hydroxylase by halogenated and nonhalogenated aromatic hydrocarbons in embryonic tissues and cells. Mol Pharmacol 40(5):818-26. PubMed: 1658612 MGI: J:2134
Kennedy GD; Nukaya M; Moran SM; Glover E; Weinberg S; Balbo S; Hecht SS; Pitot HC; Drinkwater NR; Bradfield CA. 2014. Liver tumor promotion by 2,3,7,8-tetrachlorodibenzo-p-dioxin is dependent on the aryl hydrocarbon receptor and TNF/IL-1 receptors. Toxicol Sci 140(1):135-43. PubMed: 24718703 MGI: J:215349
Kerley-Hamilton JS; Trask HW; Ridley CJ; Dufour E; Lesseur C; Ringelberg CS; Moodie KL; Shipman SL; Korc M; Gui J; Shworak NW; Tomlinson CR. 2012. Inherent and benzo[a]pyrene-induced differential aryl hydrocarbon receptor signaling greatly affects life span, atherosclerosis, cardiac gene expression, and body and heart growth in mice. Toxicol Sci 126(2):391-404. PubMed: 22228805 MGI: J:183715
Klinefelter K; Hooven MK; Bates C; Colter BT; Dailey A; Infante SK; Kania-Korwel I; Lehmler HJ; Lopez-Juarez A; Ludwig CP; Curran CP. 2018. Genetic differences in the aryl hydrocarbon receptor and CYP1A2 affect sensitivity to developmental polychlorinated biphenyl exposure in mice: relevance to studies of human neurological disorders. Mamm Genome 29(1-2):112-127. PubMed: 29197979 MGI: J:259801
Kouri RE; Rude TH; Joglekar R; Dansette PM; Jerina DM; Atlas SA; Owens IS; Nebert DW. 1978. 2,3,7,8-tetrachlorodibenzo-p-dioxin as cocarcinogen causing 3-methylcholanthrene-initiated subcutaneous tumors in mice genetically 'nonresponsive' at Ah locus. Cancer Res 38(9):2777-83. PubMed: 679184 MGI: J:84318
Levova K; Moserova M; Nebert DW; Phillips DH; Frei E; Schmeiser HH; Arlt VM; Stiborova M. 2012. NAD(P)H:quinone oxidoreductase expression in Cyp1a-knockout and CYP1A-humanized mouse lines and its effect on bioactivation of the carcinogen aristolochic acid I. Toxicol Appl Pharmacol 265(3):360-7. PubMed: 22982977 MGI: J:192865
Lew BJ; Manickam R; Lawrence BP. 2011. Activation of the aryl hydrocarbon receptor during pregnancy in the mouse alters mammary development through direct effects on stromal and epithelial tissues. Biol Reprod 84(6):1094-102. PubMed: 21270426 MGI: J:173706
Moriguchi T; Motohashi H; Hosoya T; Nakajima O; Takahashi S; Ohsako S; Aoki Y; Nishimura N; Tohyama C; Fujii-Kuriyama Y; Yamamoto M. 2003. Distinct response to dioxin in an arylhydrocarbon receptor (AHR)-humanized mouse. Proc Natl Acad Sci U S A 100(10):5652-7. PubMed: 12730383 MGI: J:132380
Nebert DW; Atlas SA; Guenthner TM; Kouri RE. 1978. The Ah locus: genetic regulation of the enzymes which metabolize polycyclic hydrocarbons and the risk of cancer. In: Polycyclic Hydrocarbons and Cancer: Chemistry, Molecular Biology and Environment. Academic Press, New York. MGI: J:30693
Nebert DW; Considine N; Owens IS. 1973. Genetic expression of aryl hydrocarbon hydroxylase induction. VI. Control of other aromatic hydrocarbon-inducible mono-oxygenase activities at or near the same genetic locus. Arch Biochem Biophys 157(1):148-59. PubMed: 4716952 MGI: J:84313
Nebert DW; Gelboin HV. 1969. The in vivo and in vitro induction of aryl hydrocarbon hydroxylase in mammalian cells of different species, tissues, strains, and developmental and hormonal states. Arch Biochem Biophys 134(1):76-89. PubMed: 4981257 MGI: J:84248
Nebert DW; Gielen JE. 1972. Genetic regulation of aryl hydrocarbon hydroxylase induction in the mouse. Fed Proc 31(4):1315-25. PubMed: 4114109 MGI: J:5282
Nebert DW; Gielen JE; Goujon FM. 1972. Genetic expression of aryl hydrocarbon hydroxylase induction. 3. Changes in the binding of n-octylamine to cytochrome P-450. Mol Pharmacol 8(6):651-66. PubMed: 4118364 MGI: J:84251
Nebert DW; Goujon FM; Gielen JE. 1972. Aryl hydrocarbon hydroxylase induction by polycyclic hydrocarbons: simple autosomal dominant trait in the mouse. Nat New Biol 236(65):107-10. PubMed: 4502804 MGI: J:84249
Nebert DW; Jensen NM. 1979. Benzo[a]pyrene-initiated leukemia in mice. Association with allelic differences at the Ah locus. Biochem Pharmacol 28(1):149-51. PubMed: 758905 MGI: J:6074
Nebert DW; Jensen NM; Shinozuka H; Kunz HW; Gill TJ 3rd. 1982. The Ah phenotype. Survey of forty-eight rat strains and twenty inbred mouse strains. Genetics 100(1):79-87. PubMed: 7095422 MGI: J:6809
Nebert DW; Kon H. 1973. Genetic regulation of aryl hydrocarbon hydroxylase induction. V. Specific changes in spin state of cytochrome P 450 from genetically responsive animals. J Biol Chem 248(1):169-78. PubMed: 4348203 MGI: J:84311
Nebert DW; Robinson JR; Niwa A; Kumaki K; Poland AP. 1975. Genetic expression of aryl hydrocarbon hydroxylase activity in the mouse. J Cell Physiol 85(2 Pt 2 Suppl 1):393-414. PubMed: 1091656 MGI: J:84317
Niwa A; Kumaki K; Nebert DW; Poland AP. 1975. Genetic expression of aryl hydrocarbon hydroxylase activity in the mouse. Distinction between the 'responsive' homozygote and heterozygote at the Ah locus. Arch Biochem Biophys 166(2):559-64. PubMed: 1119809 MGI: J:84316
Oesch F; Morris N; Daly JW. 1973. Genetic expression of the induction of epoxide hydrase and aryl hydrocarbon hydroxylase activities in the mouse by phenobarbital or 3-methylcholanthrene. Mol Pharmacol 9(5):629-6. PubMed: 4788156 MGI: J:25852
Okey AB; Vella LM; Harper PA. 1989. Detection and characterization of a low affinity form of cytosolic Ah receptor in livers of mice nonresponsive to induction of cytochrome P1-450 by 3-methylcholanthrene. Mol Pharmacol 35(6):823-30. PubMed: 2543914 MGI: J:27899
Poel WE; Stanton D; Peters E; Wade HO. 1958. Comparative susceptibilities of seven inbred strains of mice to qualified applications of 3, 4-benzpyrene Proc Am Assoc Cancer Res 2:335. MGI: J:84245
Poland A; Bradfield C. 1992. A brief review of the Ah locus. Tohoku J Exp Med 168(2):83-7. PubMed: 1339107 MGI: J:12546
Poland A; Glover E. 1990. Characterization and strain distribution pattern of the murine Ah receptor specified by the Ahd and Ahb-3 alleles. Mol Pharmacol 38(3):306-12. PubMed: 2169579 MGI: J:34840
Poland A; Glover E; Kende AS. 1976. Stereospecific, high affinity binding of 2,3,7,8-tetrachlorodibenzo-p-dioxin by hepatic cytosol. Evidence that the binding species is receptor for induction of aryl hydrocarbon hydroxylase. J Biol Chem 251(16):4936-46. PubMed: 956169 MGI: J:84247
Poland A; Glover E; Taylor BA. 1987. The murine Ah locus: a new allele and mapping to chromosome 12. Mol Pharmacol 32(4):471-8. PubMed: 2823093 MGI: J:8895
Poland A; Palen D; Glover E. 1994. Analysis of the four alleles of the murine aryl hydrocarbon receptor. Mol Pharmacol 46(5):915-21. PubMed: 7969080 MGI: J:22144
Poland A; Teitelbaum P; Glover E; Kende A. 1989. Stimulation of in vivo hepatic uptake and in vitro hepatic binding of [125I]2-lodo-3,7,8-trichlorodibenzo-p-dioxin by the administration of agonist for the Ah receptor. Mol Pharmacol 36(1):121-7. PubMed: 2546046 MGI: J:126377
Poland AP; Glover E; Robinson JR; Nebert DW. 1974. Genetic expression of aryl hydrocarbon hydroxylase activity. Induction of monooxygenase activities and cytochrome P1-450 formation by 2,3,7,8-tetrachlorodibenzo-p-dioxin in mice genetically 'nonresponsive' to other aromatic hydrocarbons. J Biol Chem 249(17):5599-606. PubMed: 4370044 MGI: J:84314
Quintana FJ; Basso AS; Iglesias AH; Korn T; Farez MF; Bettelli E; Caccamo M; Oukka M; Weiner HL. 2008. Control of T(reg) and T(H)17 cell differentiation by the aryl hydrocarbon receptor. Nature 453(7191):65-71. PubMed: 18362915 MGI: J:136052
Robinson JR; Considine N; Nebert DW. 1974. Genetic expression of aryl hydrocarbon hydroxylase induction. Evidence for the involvement of other genetic loci. J Biol Chem 249(18):5851-9. PubMed: 4413562 MGI: J:84315
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Schmid FA; Elmer I; Tarnowski GS. 1969. Genetic determination of differential inflammatory reactivity and subcutaneous tumor susceptibility of AKR-J and C57BL-6J mice to 7,12-dimethylbenz- [a]anthracene. Cancer Res 29(8):1585-9. PubMed: 5807232 MGI: J:34134
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Genetic overview

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Additional Information

Selected References

Ahrd

Allele Symbol: Ahrd

KitlSl

Allele Symbol: KitlSl

Pde6brd1

Allele Symbol: Pde6brd1

Disease Terms

Research Areas By Genotype

This mouse can be used to support research in many areas including:

Genotype: Ahrd related

Genotype: KitlSl related

Genotype: Pde6brd1 related

Mammalian Phenotype Terms by Genotype

Genotype: KitlSl/Kitl+either: (involves: C3H * WC) or (involves: C3H * C57BL/6 * DBA/2J * WC)

hematopoietic system phenotype

immune system phenotype

Genotype: KitlSl/Kitl+involves: C3H

pigmentation phenotype

hematopoietic system phenotype

hearing/vestibular/ear phenotype

reproductive system phenotype

craniofacial phenotype

integument phenotype

growth/size/body region phenotype

Genotype: KitlSl/Kitl+involves: 129/Sv * C3H

endocrine/exocrine gland phenotype

reproductive system phenotype

neoplasm

Genotype: KitlSl/KitlSlinvolves: C3H

mortality/aging

nervous system phenotype

hematopoietic system phenotype

cardiovascular system phenotype

reproductive system phenotype

pigmentation phenotype

embryo phenotype

integument phenotype

References

Additional References

Additional - Ahrd related

Additional - KitlSl related

Additional - Pde6brd1 related

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Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200

Live Mouse

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Credit for PRODUCTS or SERVICES

Animal Care and Use for SERVICES

No Liability

Ahr^d

Allele Symbol: Ahr^d

Kitl^Sl

Allele Symbol: Kitl^Sl

Pde6b^rd1

Allele Symbol: Pde6b^rd1

Genotype: Ahr^d related

Genotype: Kitl^Sl related

Genotype: Pde6b^rd1 related

Genotype: Kitl^Sl/Kitl⁺
either: (involves: C3H * WC) or (involves: C3H * C57BL/6 * DBA/2J * WC)

Genotype: Kitl^Sl/Kitl⁺
involves: C3H

Genotype: Kitl^Sl/Kitl⁺
involves: 129/Sv * C3H

Genotype: Kitl^Sl/Kitl^Sl
involves: C3H

Additional - Ahr^d related

Additional - Kitl^Sl related

Additional - Pde6b^rd1 related